This Is MS Multiple Sclerosis Community: Knowledge & Support

You hit the nail on the head again Nigel.

No one has all the answers and many of you have permanent structural and neurological damage that will limit the outcome of even the best intervention. There are new options to consider, however. Venous liberation has certainly turned some heads. Even if the improvemets didn't last long in every case some of the changes have been remarkable. Specific chiropractors have something significant to bring to the table as well and can only improve what is being done with CCSVI intervention by removing potential musculoskeletal problems in a way any scientist or physician can relate to. Neurosurgeons and some other specialists are also coming up with some excellent minimally invasive options such as endoscopic surgery which is a serious consideration in Blossom's case. Radiologists are ready now to check blood and CSF flow as well as structure to determine possible cause as well as to test the effectiveness of intervention. Duplex ultrasound is another excellent monitoring device. The trick is determinig how to best apply what we know so far.

My guess is that no matter whose theory is right we are on the right path and patients will win in the end. What's more, the time and technology is here now.

you have explained the situation very well , dear Dr.Upright.

I would like to add this if I may ......

MrSuccess is a very strong believer in MS being triggered by Trauma. I base my opinion
on this theory ...... as a result of the research work of respected medical professionals.

It is estimated that about - 6 % - of previously healthy people that suffer some form of head , neck , or back TRAUMA ....... then go on to develop..... MS -like symptoms......

Dr.Zamboni's discovery certainly looks like the missing part of the puzzle.

Putnam's dogs ? ........ No need ..... we now have human proof.



MrSuccess

Thanks Mr. Success.
The case below is from my wordpress blog. It is another example of a bicycle accident that resulted in migraines and MS.

I have read everything including anecdotal stories that has given me a strong aha moment in regard to head, spine injuries.
Age 9/10 i had a bicycle accident where i flew over handlebars for about 3-4 ft into the sidewalk facefirst. i lost conciousness and came too with temporary amnesia; i passed out again and i came to in my grandmothers kitchen with an icepack on my face. No hospital visit was made.
Age 17-21 (1977-1981); episodes of leg weakness, double vision and after pregnancy i deteriorated to almost complete body weakness with limbs, including neck, back collapse due to extreme muscle weakness, couldn’t chew or swallow, etc… Diagnosed at age 21 by my son’s neurologist with myasthenia gravis and was treated with mestinon and a thymectomy. 3 years later back to normal. MG in remission.

1996 i had numbness in the bottom of my feet that moved up the legs to waist with weaness. Took 6 months off work and recovered.

2001 i developed pars planitis and was treated with prednisone which eventually caused bout with optic neuritis and almost full paralysis which lasted for 3 months until ms diagnosis which showed lesions in brain and spinal cord.
2004 i left work as my ms fatigue, vertigo, dizziness, throat weakness causing aspiration pneumonia and am now on LTD. I have continued to deteriorate and my left leg is very weak and spastic; both arms and hands weak and bouts with jerky tremors frequent. Also severe migraines increasing as well as 2 ruptured disks (c5) and also lower back but i can’t remember which disc.
I would very much welcome your thoughts and comments. I live in Toronto, Ontario, Canada.

dr. flanagan,

on the lighter side, the little discussion we kinda had about finding hens teeth. your come back was great and on the money. growing up a farm girl, i can barely eat and rarely eat as i refer to as factory eggs. unless people have experienced good food i think most don't realize what and just how bad our food chain has become. but those of us do what we can, when we can and how we can and of course what is affordable and available individually.

anyhow, how does this "chicken egg thing" connect in anyway to ccsvi?? i feel very much. how?--well, figureing out all this is kinda trying to figure out--which came first--the chicken or the egg!! ????????????????????????????????????????????????????

you are welcome URD . I urge all pwMS to take some time and research the connection between MS and TRAUMA. Just enter MS and TRAUMA into any search engine.

You will discover that this association has long been suspected . Long before MRI's. Long before MRV's. It goes back over 30 years ago. Back to the old day's when doctors had to remember their patients names , their health condition ...... and just plain and simple ... act like a detective.

Let's do an experiment .

Pick an arm. Pick a leg. Now have someone clobber this appendage. HARD. I guarantee you that the inflicted trauma ..... will result in INFLAMMATION. The arm , leg or whatever will SWELL and get LARGER.

Let's do another experiment .

This time ..... we induct TRAUMA to the NECK. We again have INFLAMMATION. However , this is different ..... the inflammation ..... is INTERNAL . The resulting SWELLING acts like a hand squeezing a finger. This results in the crushing of those delicate [ mostly female] and vital brain drainage pathways . For many [ estimated 94% ] when the swelling subsides .... the drainage veins return to normal. For the unlucky few [ estimated 6% ] their veins remain blocked . They soon go on to have MS. But it takes time. Never overnight.

And the CCSVI theory certainly dovetails nicely into the great mystery of the WHY - some- previously healthy people go on to have MS .... AFTER .. an incident of TRAUMA.


It's a theory ...... but so is the " malfunctioning immune system THEORY "


If not for differences of opinion ...... we would not have horse races ....



MrSuccess

Good question Blossom,
It takes a lot of energy and nutrition to make a good eggshell. It likewise takes a lot of energy and nutrition to make bones. In particular, it takes calcium and vitamen D. There is an old wive tale that said, "A tooth for every child" because pregnancy requires extra calcium and vitamen D. If it is not supplied by the diet the body will take it out of the bones. The parathyroid glands control calcium levels between bone and blood. Among other things, a lack of sunshine vitamen D causes a decrease in bone production and an increase in bone breakdown that can result in rickets or osteomalacia - bad bones. People living in smog laden cities and those who avoid the sun for other reasons can get weak bones due to decreased vitamen D. Rickets causes bow legs and hunched backs due to bone collapse.

The egg cycle in naturally raised chickens is tied to sunlight and the length of day which is clocked by the pineal gland attached to the third ventricle. Winter is a yin time of year. It is a time of consolidation and restoration. When sun and food are in short supply the smart naturally raised ladies prefer to sleep longer in the roost and produce less. They don't care how much the rooster crows to get up in the morning. Conveyor belt chickens are raised under artificial lights and constant feed to squeeze more eggs and food out of them. Their weak shells and wimpy egg whites show it.

The moral of the story is that a lack of vitamen D affects the bones. On the other hand, excess vitamen D may play a role in kidney stones.

The following is from comments on my wordpress blog regarding a case of whiplash, a Chiari malformation with a syrnix in the cord and MS.

Help! I will try to keep this short and sweet. At age 14 my daughter was in an automobile accident suffering from neck & back pain, and severe daily headaches. (she was twisted at the waist, turning to talk to the girl behind her when the car was struck) From that night forward she has not been the same. Ten years later we finally got an MRI because her pupils were uneven. The MRI revealed Chari I Malformation. Nothing was done until they finally, a year later, discovered a lesion/syrinx on her spinal column which indicated restricted CSF. She finally had decompression surgery in October 2010. But, In addition to the uneven pupils and the symptoms described above. She has had many strange symptoms that doctors say are not related………falling down at times, difficulty swallowing or chocking, severe stomach pains, irregular menstrual cycles, cold hands & feet with discoloration, tingling and numbness. (diagnosed with reynauds last week) Recently, all of her hormones tested below the levels of a menopausal women. (appear to be normal now) Her thyroid was supposedly not functioning. Prescribed medication by one doctor only to be taken off by another. My question to you; Is there any correlation between any of these symptoms? We had our last visit with the neuro-surgeon yesterday. The syrinx in the upper spine appears to be gone according to the latest MRI. However, they have never looked at her entire spine. Could there be something going on that they’ve missed? Something that could explain some of these other symptoms? I should also reveal that her grandfather (on her father’s side) had Parkinson’s and a cousin has MS.
Worried Mom!

Hi all, I could only just read/see what Sal has said and it seemed to me that it has significance for Dr. F.

" In an arrested development in the J3 region, there will be an effect on the jugular canal. Remember that the veins of the dural sinuses and the internal jugular vein are a continuous conduit. The bones of the skull grow around these vascular and neural structures, leaving holes in the bones (canals and foramina) through which the blood vessels and neural tissue travel. If the vein is small during bony development, the canal will be small and there will be little opportunity for expansion of venous foramina at a later date.
One clue in differentiating these two circumstances is the size of the condylar emissary veins. These veins were part of the fetal circulation that is supposed to atrophy as the adult system develops the jugular vein. If jugular hypoplasia occurs, then condylar emissary vein flow dominates and the condylar fossa is enlarged considerably. This is an important observation.
Angioplasty of a hyoplastic vein in a narrow canal will do nothing but injure the small vein. Angioplasty obviously cannot dilate bony canals. So if there is a hypoplasia, at the skull neck junction, I tend to leave this alone. On the other hand, a recanalized occlusion may look hypoplastic but often has collateral veins outside the skull. Often the jugular bulb and the jugular canal are normal in size. This can be treated by angioplasty and, if necessary by a stent, (timing considerations for stenting as previ,ously described.)"

https://www.facebook.com/Sal.Sclafani.M ... 8890834465
Re some thing
Nigel

Dr. F, the out comes for all of these people including me are what we need to understand.

Why is there a problem, what is the cause, and how can we manage it!

My two children, now young adults have just arrived after six years of separation and I am seeing things differently. Its like my eyes are more open, type of thing.
I hear that Sal and others are at a lost as to why outcomes are so variable, I also hear how there may be a causation from you. But to a person like me, stuck in logic, trying to make 'sense',
but as yet no one has an understanding of what all these symptoms are about!

There are links to injury, to vascular malformation, genealogy, hereditary, diet, latitude the neighbors cat and we are not there yet, and I can barely see this so I will end now.

And more importantly, how are you? Have you come through the recent gathering with good health?
Gards all,
Nigel

The following comment from my wordpress blog was in response to the previously posted case involving a Chiari malformation and MS following trauma.

While I can’t speak for all of your daughter’s “strange symptoms” I can tell you without doubt that some of the symptoms she is/was experiencing is related to the CM1 diagnosis. I know this without doubt because I too have CM1 for which I underwent surgery. I had many of the same symptoms as your daughter; the falling down, difficulty swallowing/choking, tingling/numbness. During the long, drawn out process of finding the correct diagnosis for my symptoms, I also was tested for thyroid problems. My symptoms also started as the result of related trauma but research states that many people probably have the CM1 condition but until a trauma of some type happens, the condition does not affect the person. Given that only approximately 3% of the US population is ever truly diagnosed with CM1, it is commonly overlooked or mis-diagnosed. Luckily I was blessed with a fabulous neurosurgeon who didn’t “jump the gun” and diagnose me with MS which is so often the case. I do however find it interesting that you have a family history of MS. This is interesting to me because years after my diagnosis of CM1, my brother was diagnosed with MS. His neurologist assures us that CM1 was ruled out as a possibility for his symptoms but since him and I are the only 2 people in our entire family (that anyone can remember) with any neurological conditions, we are convinced that MS and CM1 must somehow be related.

If your daughter has presistant symptoms, I would re-visit the neurosurgeon or get a 2nd opinion. Research also shows that some patients require additional surgeries/decompression

I would have to agree. As I have said before on this thread, it may make sense to increase the capacity of the veins without problems than to try and increase flow through veins with cranial obstructions such as foraminal hypoplasia. I have a demo skull on my desk that shows similar bone modeling problems due to craniosynostosis (premature closing of the sutures). The sigmoid sinus and hypoglossal canals are smaller on the left and the condylar canal is absent. The right side has an extra large sigmoid sinus, jugular foramen, hypoglossal and condylar canals. The sutures of the skull are wide open on the left suggesting intracranial pressure due to hydraulic stress. On the right side the sutures are obliterated due to craniosynostosis.

When it comes to the development of the blood and CSF circulatory pathways in the brain I have a different opinion but it is too lenghty to go into here. Suffice it to say that Schelling began his research when noted that MS patients had a discrepancy in the size of their jugular foramen. I will be discussing in utero bone modeling issues that may play a role in conditions sucha Dandy Walker syndromes, Chiari malformations, hydrocephalus etc. as my website grows. Dandy-Walker syndromes are sort of like a reverse Chiari malformation. Both conditions affect females far more than males. It most likely has to do with the design of the posterior fossa. Among other things, Dandy-Walker are associated with hydrocephalus and an enlarged posterior fossa and foramen magnum. Instead of sinking into the foramen magnum the cerebellum gets pushed up into the tentorium cerebelli (the cover over the posterior fossa and cerebellum).

It's a question of which comes first, the chicken or the egg. The blood and CSF circulatory pathways develop along with the skull and problems in the development of one can affect the other. In addition to genetics, I suspect in utero events can block circulatory pathways and affect development and final design.

Nigel,
According to my theory, brain and cord problems can be caused by a myriad of inherited (Klepell-Feil, craniosysnostosis, Chiari malformation, Dandy-Walker syndromes, atlantooccipital assimilation, block vertebra, scoliosis, tethered cord as well as many, many other design problems) and acquired (aging and injuries), such as spondylosis, scoliosis and stenosis, can compress nerves, blood vessels and CSF circulatory pathways. Humans are susceptible to these conditions by design.

No one questions the science that stenosis of the intervertebral formen compresses nerve roots which cause pain, weakness and decreased reflexes. No one questions the science of behind canal stenosis and compressive myelopathy of the cord. My theory simply expands on sound existing science.

I read a theory by someone who did a presentation on MS shortly after one given by Haake. The theory had to do with neurodegenerative diseases being caused by humans resorting to wearing shoes. He postulated that wearing shoes resulted in a loss of grounding and lot of fancy footwork type explanations of how it resulted in neurodegenerative processes and subsequent diseases such as MS. I read through it quickly because it didn't interest me in the least. It was full of flaws in science and reasoning. I am not even remotely interested in debating the topic except suffice it to say that if Eskimos, who don't get MS anyway despite wearing shoes, but if they didn't wear shoes they would die of frostbite long before middle age when most neurodegenerative diseases start to show up. You have to prioritize research projects. You have to convince people to invest in your theory which should be based on reasonable evidence and biological plausibility. Some theories just don't make sense and some are really far fetched.

As for the weekend - an interesting turn of events happened. The trigeminal neuralgia, facial swelling, jaw pain, leg and arm tremors, paraesthesias, sleeplessness, dry mouth, burning tongue, cheek and jaw pain, right leg weakness and spasms etc all returned, all because of a simple local surgical procedure. Fortunatly for me, I know what caused it how to best deal with the classic adverse reactions mentioned above. Unfortunatly, it may have also done some permanent damage to bone.

Knowing the cause is always helpful in determining treatment. Despite what I know, it took a couple of years to figure out the cause in my case. The link between cause and effect, however, wasn't clear because I was never informed as a consumer about a new product used in my case and its possible nasty side effects. In hindsight, it was plain as day and it should have been obvious considering my background knowlege in neurotoxins. This isn't the first time. This time there is a long trail of very strong circumstantial evidence, witnesses and physiological signs all pointing right back to the culprit caught "red handed" at the scene of the crime. It is an interesting story but not for here, and not fun for me. Some people have some serious explaining to do.

DR. FLANAGAN,

from the chicken or the egg questions to so many things. you know my stand when it comes at least to my case. "the spine".
but, to throw more into the mix: noone on either side of my family as far back as i could check. - but, my x's first wife had ms. his first cousin has ms.

i have been a real hit with the neuro's through the yrs. always questioning and wanting them to look further with my spine and me being told it would not have anything to do with my symptoms. from the get go.

i questioned the fact about the x's first wife with ms and could there be a chance maybe he was like a "typhoid mary" a carrier and the extreme stress i was usually under and then the fall i took weakened me and it popped up in me.---was told ms was not sexually transmitted. i asked just what do they think causes ms--was told they thought it was as virus. my come back was-ok you're telling me you feel ms is caused by a virus but is not sexually transmitted but aids is a virus and is sexually transmitted. there are a few dr.'s i've read about that feel it is a possibility.----soooo, trauma was not the cause nor was it possible to transmit ms.????????????????????????????????????

and, how many yrs. has it been and it seems in a lot of ways at times we are still like a cat chaseing it's tail.

there are many people with these symptoms they named ms and i don't think we all will follow the same exact path.

BUT THE SPINE SEEMS TO ME THE BEST PATH TO START WITH.

Well put Blossom,
The problem is in the definition and the terminology. Classically MS is associated with multiple scars in the surpratentorial, periventricular and perivenular areas of the brain. The problem got started with Charcot who was simply describing the pathology (lesions in the brain and cord) associated with the other signs and symptoms of the condition.

As you know, you don't have definite MS. You have probable MS because you have the signs and symptoms but you lack classic lesion locations in the brain. Instead, like costume national and many others you have lesions in your upper cord, which disqualifies you from having definite MS. You don't have cervical spondylotic myelopathy yet either but again you have similar signs and symptoms.

Asian and African people have a much lower incidence of MS. On the other hand they do get Devic's and optic spinal multiple sclerosis which can be worse. These condition are not considered to be MS because they get optic neuritis and transverse myelitits (lesions in the cord) instead of brain lesions. I believe it is due to design differences in the skull, especially the posterior fossa. The posterior fossa takes the brunt of inversion flows and sluggish flow.

It is my opinion that they are all the same condition due to similar causes with slightly different outcomes in clinical findings; that is, the lesions show up in different places. Compressive spondylotic myelopathy not only mimics MS but I believe it can cause it.

Another RLS/massage update: Yesterday's massage using the same routine (lower pillow, head turned the opposite way) was RLS-free! Three great visits in a row, after months & months of leg-spasm-filled massages. Yes, in my case RLS does seem to have a correlation with my (already diagnosed) upper cervical damage - hope to get my UC examined soon.

And again, I wish everyone a relaxing, pain free day today.

_________________
Dx'd with MS & HNPP (hereditary peripheral neuropathy) 7/03 but must have had MS for 30 yrs before that. I've never taken meds for MS or MS symptoms except 1 yr experiment on LDN. (I found diet, exercise, sleep, humor, music help me the most.)